Pain
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The aims of the present analysis were to investigate the short- and long-term efficacies and treatment moderators of psychological interventions for fibromyalgia. A literature search using PubMed, PsychINFO, the Cochrane Library, and manual searches identified 23 eligible studies including 30 psychological treatment conditions and 1396 patients. Meta-analytic integration resulted in a significant but small effect size for short-term pain reduction (Hedges's g=0.37, 95% confidence interval (CI): 0.27-0.48) and a small-to-medium effect size for long-term pain reduction over an average follow-up phase of 7.4 months (Hedges's g=0.47, 95% CI: 0.3-0.65) for any psychological intervention. ⋯ Publication-bias analyses demonstrated that the effect sizes were robust. The results suggest that the effects of psychological treatments for fibromyalgia are relatively small but robust and comparable to those reported for other pain and drug treatments used for this disorder. Cognitive-behavioral therapy was associated with the greatest effect sizes.
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The primary purpose of the present study was to examine the temporal stability of communicative and protective pain behaviors in patients with chronic back pain. The study also examined whether the stability of pain behaviors could be accounted for by patients' levels of pain severity, catastrophizing, or fear of movement. Patients (n=70) were filmed on two separate occasions (i.e., baseline, follow-up) while performing a standardized lifting task designed to elicit pain behaviors. ⋯ Regression analyses also showed that pain behaviors remained stable when accounting for patients' levels of catastrophizing and fear of movement. Discussion addresses the potential contribution of central neural mechanisms and social environmental reinforcement contingencies to the stability of pain behaviors. The discussion also addresses how treatment interventions specifically aimed at targeting pain behaviors might help to augment the overall impact of pain and disability management programs.
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A novel cell-cell signaling by microglial transmembrane TNFα with implications for neuropathic pain.
Neuropathic pain is accompanied by neuroimmune activation in dorsal horn of spinal cord. We have observed that in animal models this activation is characterized by an increased expression of transmembrane tumor necrosis factor α (mTNFα) without the release of soluble tumor necrosis factor α (sTNFα). Herein we report that the pain-related neurotransmitter peptide substance P (SP) increases the expression of mTNFα without the release of sTNFα from primary microglial cells. ⋯ In order to evaluate the biological function of uncleaved mTNFα, we transfected COS-7 cells with a mutant full-length TNFα construct resistant to cleavage by TACE. Coculture of COS-7 cells expressing the mutant TNFα with microglial cells led to microglial cell activation indicated by increased OX42 immunoreactivity and release of macrophage chemoattractant peptide 1 (CCL2) by direct cell-cell contact. These results suggest a novel pathway through which the release of SP by primary afferents activates microglial expression of mTNFα, establishing a feed-forward loop that may contribute to the establishment of chronic pain.
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Conditioning procedures are used in many placebo studies because evidence suggests that conditioning-related placebo responses are usually more robust than those induced by verbal suggestions alone. However, it has not been shown whether there is a causal relation between the number of conditioning trials and the resistance to extinction of placebo and nocebo responses. Here we test the effects of either one or four sessions of conditioning on the modulation of both non-painful and painful stimuli delivered to the dorsum of the foot. ⋯ However, these effects extinguished over time. Conversely, four sessions of conditioning (Group 2) induced robust placebo and nocebo responses to both non-painful and painful stimuli that persisted over the entire experiment. These findings suggest that the strength of learning may be clinically important for producing long-lasting placebo effects.